Rheumatoid arthritis (RA) has been described as an unresolved systemic inflammation in which immune dysfunction and genetic susceptibility play roles. In earlier stages it is characterized by fluctuating remissions and exacerbations, and in later stages by a chronic granulatomous response (panus formation) leading to tissue destruction. The synovial membrane in RA has many of the characteristics of a hyperactive immunologically stimulated lymphoid organ and the ratio of T suppressor to T helper lymphocytes has been shown to be significantly reduced.
Although a number of attempts have been made to implicate bacteria, viruses and mycoplasms as etiological agents, no specific causative agent has been clearly proven. It is possible that there is no specific etiological agent, and that the important agent or factor may be the result of an interplay of hereditary factors and physiological changes on non-specific inflammatory states.
A great deal of work has been expended on the late, destructive phase of this disease in which anaphylactically induced leukotrienes and prostaglandins may play a chemotactic role in migration of neutrophils and macrophages into the rheumatoid synovium leading to destruction of bone and cartilage. Many attempts have been made to intervene between these events and the subsequent destructive phase occurring in the rheumatoid synovia.
Since there is no unambiguous test distinguishing RA from other acute or chronic inflammatory diseases, differentiating RA from other arthritides, such as systemic lupus erythematosus, (SLE) ankylosing spondylitis, (AS), polyarticular gout (PAG), psoriatic arthritis (PsA), etc., is often difficult. Diagnosis of RA is usually made according to American Rheumatism Association (ARA) criteria. As seen from Table 1, a patient whose symptoms meet at least 3 of the 8 criteria is considered probably to have RA, while a definite clinical diagnosis is usually not made until 5 or more of the symptoms are positive. However, it is not unusual for diagnoses to be changed after further observations, since complications in diagnosis may result from overlapping symptoms, and the presence of symptoms from one arthritides does not preclude the possibility that the patient may also have another arthritic disease.